ARTHRITIS
AND THE GLUTATHIONE CONNECTION
AND THE GLUTATHIONE CONNECTION
Live long enough and you can pretty much count on developing arthritis: a touch of osteoarthritis, at the very
least.
Arthritis ('arth' meaning joint, 'itis' meaning inflammation) isn't a one-note story or even a few variations on a
single theme; it actually consists of more than 100 different conditions. These can be anything from relatively
mild forms of tendinitis (as in 'tennis elbow') and bursitis to crippling systemic forms, such as rheumatoid
arthritis. There are pain syndromes like fibromyalgia and arthritis-related disorders, such as systemic lupus
erythematosus, that involve every part of the body. There are forms of the disease, such as gout, that almost
nobody connects with arthritis, and there are other conditions - like osteoarthritis, the misnamed 'wear and tear'
arthritis - that a good many people think is the only form of the disease.
True, many older people do have arthritis, but it's not just a disease of the old. Some forms of arthritis affect
children still in diapers, while thousands of people are stricken in the prime of their lives. The common
denominator for all these conditions is joint and musculoskeletal pain, which is why they are grouped together
as 'arthritis.' Often that pain is a result of inflammation of the joint lining.
Inflammation is involved in many forms of arthritis. It is the body's natural response to injury. The warning
signs that inflammation presents are redness, swelling, heat and pain. These are the same kinds of reaction the
body has to a sliver in the hand, for example. When a joint becomes inflamed, it may get any or all of these
symptoms. This can prevent the normal use of the joint and therefore it can cause the loss of function of that
joint.
Anatomy of a Joint
There are more than 100 joints connecting the body's
206 bones. Most of the major bone connections in the
body are joints designed to allow a broad range of motion.
There are different kinds for different functions:
ball-and-socket (hips and shoulders), saddle joints (which
connect thumb to hand), hinge joints (fingers and knees)
or pivot joints (wrists).
Tied together by ligaments, the bones of joints are capped
with a smooth substance called cartilage. This tough elastic
material acts as a shock absorber and allows the bone ends
to glide smoothly across each other. If the cartilage is
destroyed (as in osteoarthritis), the bones of a joint can
grind against each other causing pain, loss of mobility, deformity and dysfunction.
Between the bones is a joint cavity, which gives the bones room to move. The joint space between two bones
is enclosed by a capsule that's flexible, yet strong enough to protect the joint against dislocation. The inner
lining of this capsule, the synovium, produces a thick fluid that lubricates and nourishes the joint. In many forms
of arthritis, the synovium becomes inflamed and thickened, producing extra fluid which contains inflammatory
cells. The inflamed synovium and fluid can damage the cartilage and underlying bone.
Some people think that there are only a couple of kinds of Arthritis, However make no mistake.... there are 100
FOLD and probably more to be added to this list.......
Achilles tendinitis Achondroplasia Acromegalic arthropathy
Adhesive capsulitis
Adult onset Still's disease Ankylosing spondylitis Anserine bursitis
Avascular necrosis
Behcet's syndrome Bicipital tendinitis Blount's disease
Brucellar spondylitis
Bursitis Calcaneal bursitis Calcium pyrophosphate dihydrate (CPPD)
Crystal deposition disease Caplan's syndrome Carpal tunnel syndrome
Chondrocalcinosis
Chondromalacia patellae Chronic synovitis Chronic recurrent multifocal osteomyelitis
Churg-Strauss syndrome Cogan's syndrome Corticosteroid-induced osteoporosis
Costosternal syndrome CREST syndrome Cryoglobulinemia
Degenerative joint disease
Dermatomyositis Diabetic finger sclerosis Diffuse idiopathic skeletal hyperostosis
(DISH)
Discitis Discoid lupus erythematosus Drug-induced lupus
Duchenne's muscular dystrophy
Dupuytren's contracture Ehlers-Danlos syndrome Enteropathic arthritis
Epicondylitis
Erosive inflammatory osteoarthritis Exercise-induced compartment syndrome
Fabry's disease Familial Mediterranean fever Farber's lipogranulomatosis
Felty's syndrome
Fibromyalgia Fifth's disease Flat feet
Foreign body synovitis
Freiberg's disease Fungal arthritis Gaucher's disease Giant
cell arteritis
Gonococcal arthritis Goodpasture's syndrome Gout Granulomatous arteritis
Hemarthrosis
Hemochromatosis Henoch-Schonlein purpura Hepatitis B surface antigen disease Hip
dysplasia
Hurler syndrome Hypermobility syndrome Hypersensitivity vasculitis
Hypertrophic osteoarthropathy
Immune complex disease Impingement syndrome Jaccoud's arthropathy Juvenile
ankylosing spondylitis
Juvenile dermatomyositis Juvenile rheumatoid arthritis Kawasaki disease
Kienbock's disease
Legg-Calve-Perthes disease Lesch-Nyhan syndrome Linear scleroderma
Lipoid dermatoarthritis
Lofgren's syndrome Lyme disease Malignant synovioma
Marfan's syndrome
Medial plica syndrome Metastatic carcinomatous arthritis Mixed connective tissue disease
(MCTD)
Mixed cryoglobulinemia Mucopolysaccharidosis Multicentric
reticulohistiocytosis
Multiple epiphyseal dysplasia Mycoplasmal arthritis Myofascial pain syndrome
Neonatal lupus
Neuropathic arthropathy Nodular panniculitis Ochronosis
Olecranon bursitis
Osgood-Schlatter's disease Osteoarthritis Osteochondromatosis
Osteogenesis imperfecta
Osteomalacia Osteomyelitis Osteonecrosis
Osteoporosis
Overlap syndrome Pachydermoperiostosis Paget's disease of bone
Palindromic rheumatism
Patellofemoral pain syndrome Pellegrini-Stieda syndrome Pigmented villonodular synovitis
Piriformis syndrome
Plantar fasciitis Polyarteritis nodos Polymyalgia rheumatica
Polymyositis
Popliteal cysts Posterior tibial tendinitis Pott's disease
Prepatellar bursitis
Prosthetic joint infectio Pseudoxanthoma elasticum Psoriatic arthritis
Raynaud's phenomenon
Reactive arthritis/Reiter's syndrome Reflex sympathetic dystrophy syndrome
Relapsing polychondritis Retrocalcaneal bursitis Rheumatic fever
Rheumatoid arthritis
Rheumatoid vasculitis Rotator cuff tendinitis Sacroiliitis
Salmonella osteomyelitis
Sarcoidosis Saturnine gout Scheuermann's osteochondritis
Scleroderma
Septic arthritis Seronegative arthritis Shigella arthritis
Shoulder-hand syndrome
Sickle cell arthropathy Sjogren's syndrome Slipped capital femoral epiphysis
Spinal stenosis
Spondylolysis Staphylococcus arthritis Stickler syndrome
Subacute cutaneous lupus
Sweet's syndrome Sydenham's chorea Syphilitic arthritis Systemic
lupus erythematosus (SLE)
Takayasu's arteritis Tarsal tunnel syndrome Tennis elbow
Tietse's syndrome
Transient osteoporosis Traumatic arthritis Trochanteric bursitis
Tuberculosis arthritis
Arthritis of Ulcerative colitis Undifferentiated connective tissue syndrome (UCTS)
Urticarial vasculitis
Viral arthritis Wegener's granulomatosis Whipple's disease
Wilson's disease
Yersinial arthritis
ARTICLE ON RHEUMATOID ARTHRITIS
- Rheumatoid Arthritis: New Discoveries Against Joint Pain and RA Symptoms
Individuals struggling with the pain and symptoms of Rheumatoid Arthritis, RA, will want to know about NEW
medical discoveries that are helping many people to significantly reduce and even clear their SYMPTOMS,
especially JOINT PAIN!
- One of these discoveries is about BALANCING instead of SUPPRESSING the immune system with immune
suppressant drugs -- and instead, how to CALM the immune and "bring it back into line" when it is "out of
whack."
- RA is considered to be an autoimmune disease, where the immune system is "over the top," and attacks the
joints, which causes pain and dysfunction -- but there is more to it!
Why Balance, Not Suppress Your Immune System?
- If you have Rheumatoid Arthritis, it is important that you know about the discovery that your immune can be
both "UNDER-active" and "OVER-active" at the same time!
- In fact, scientists have reported that with RA there are both "OVER-active" B cells and "under-active" T cells.
- This means that ... the "OVER-activity" is "PICKING ON" the joints, causing inflammation and pain.
- On the other hand, the "UNDER-activity" represents a weakened ability to deal with "ANTIGENS," i.e. to "MOP
UP" excess free radicals and "OXIDATIVE STRESS."
- This UNDER ACTIVITY also eventually results in tissue damage and increased inflammation and pain!
Best "Food for Your Immune?"
- For healing your RA, you need to both STRENGTHEN the UNDERactive parts of your immune, as well as CALM
the OVERactive immune responses.
- Just using IMMUNE SUPPRESSANT DRUGS does not really solve the problem, because this only addresses
one part of the equation.
- How to RE-BALANCE the immune to restore its natural SELF-REGULATING capacity? There is a NATURAL
DISCOVERY, a protein that improves the body's glutathione levels.
GLUTATHIONE : Why is it the key?
- Scientific data is pointing to a molecule called Glutathione as being key to the regulation of the immune
system -- both its ups AND its downs!
- In fact...there are scientists who have demonstrated a clear IMPROVEMENT OF INFLAMMATION after raising
Glutathione in affected tissues.
- Furthermore, this new discovery is noteworthy to people with Rheumatoid Arthritis now, because it has
recently become known that glutathione levels are best raised with precursors such as GSH-IMMUNITY.
Nutrition -- Not Just a Pill
- Glutathione is a fragile protein which is destroyed in stomach juices, there for pills cannot improve your
body's glutathione levels.
Dr. Bounous' "Back To Nature" Discovery:
- It was Dr. Bounous at McGill University in Montreal, who, after two decades of research, "Ended up identifying
the remarkable properties of some proteins that turned out to be the same as the three proteins in mothers’
breast milk.”
“It was a back-to-nature call,” according to Dr. Bounous.
- His discovery was -- the secret of nature to provide a cysteine-rich protein as the natural building block, or
NUTRITIONAL precursor, to making Glutathione.
- Anyone with Rheumatoid Arthritis OR ANY ARTHRITIS can benefit from this discovery by increasing their
Glutathione levels safely and naturally, with CYSTEINE-RICH protein to reduce inflammation and pain.
No Pain Killers Are Safe, Say Scientists
- Why use supplements to heal the body rather than rely on pain killers? A recent study shows that most
prescription and over-the-counter painkillers increase the risk of heart attacks. In the wake of the largest study
to date showing most nonsteroidal anti-inflammatory drugs (NSAIDs) -- including ibuprofen, naproxen, and
Celebrex -- increase the risk of heart attacks in people with arthritis, experts are once again urging all involved
to weigh their individual risks when choosing a painkiller.
- "This is a class effect of all the drugs," says researcher Gurkirpal Singh, MD, professor of medicine,
immunology, and rheumatology at Stanford University Medical School about his study presented at the Annual
European Congress of Rheumatology in Vienna, Austria.
Acetaminophen has been shown to deplete Glutathione from lung tissue.
Raynaud's Syndrome
- Raynaud’s syndrome (RS) can be a debilitating condition that causes periods of severely restricted blood flow
to the fingers and toes (and sometimes to other parts of the body such as the nose or ears). In the worst case
scenario, this can result in amputation of the damaged digits. The causes of RS remain a mystery in many cases.
-The disease causes significant free-radical nerve damage in the affected tissues. This damage leads to local
endothelial dysfunction, thickening of the arterial walls, and the formation of scar tissue, or fibrosis (Simonini G
et al 2000). RS is closely associated with more serious diseases (especially scleroderma, a connective tissue
disorder). Many scientists believe that RS may be the initial diagnosis, before the actual diagnosis of
scleroderma is recognized. Other diseases associated with RS include systemic lupus erythematosus and
arthritis.
- In each case, RS may contribute to the more serious disease by encouraging the formation of scar tissue in
the connective tissue and through damage to arteries. Therefore, it is crucial that patients who have RS pursue
aggressive ANTIOXIDANT THEARPY to lower their risk of developing a more serious condition.
- RS typically affects the small blood vessels in the fingers and toes but can affect those in the ears, nose, and
tip of the tongue as well (Adee AC 1993; Awami M et al 2004a,b; NIAMS 2001). During episodes of RS, the
affected area may become painful and turn blue (NIAMS 2001). RS that occurs in the absence of another disease
is referred to as primary RS (also sometimes called Raynaud’s disease or Raynaud’s syndrome). It is thought to
involve a localized defect in the arteries and arterioles that deliver blood to the extremities. Because RS is
associated with conditions, such as migraine headaches and angina, caused by spasms of blood vessels
(vasospasm), it may have a similar vasospastic mechanism.
- RS that occurs in the presence of other diseases is called secondary RS. Occupational RS is a common form of
secondary RS that results from using vibrating tools such as jackhammers (NIAMS 2001). Drugs or treatments
used to treat high blood pressure (beta blockers), migraine headaches (ergotamine-containing drugs), and
cancer (chemotherapy) have been known to cause RS (Merck 2005; NIAMS 2001). Oxidative Damage: RS’s
Lasting Effect
- In normal healthy tissue, blood flow to the skin is regulated by a complex system that includes neural signals,
hormones, and mediators released from circulating cells and blood vessels. Under normal circumstances, when
a person is exposed to cold or is under emotional stress, arterioles constrict to return blood flow to the core of
the body, for warmth and protection (NIAMS 2001). This reaction is regulated by vasoconstrictive agents such as
endothelin 1 (Nakamura H et al 2003; Rajagopalan S et al 2003a) and factors that impair production of nitric
oxide, a potent vasodilator (Generini S et al 2005).
-In individuals with RS, the normal reaction is exaggerated—blood circulation in the arterioles is greatly
restricted, resulting in a visible progression of symptoms as blood flow to the affected areas drops. Skin first
turns white as it is deprived of blood, then turns blue (cyanosis) because of the lack of blood and oxygen, and
then has localized red flushing as the blood returns to the affected area (Browne BJ et al 1995). This progression
may be accompanied at first by a loss of sensation in the affected extremities, followed by a prickling,
throbbing, or tingling sensation as circulation returns (NIAMS 2001).
Skin changes may migrate, moving from one finger to the next, sometimes even involving the thumb (Pistorius
MA et al 1995). The tip of the nose, the earlobes, and (rarely) the cheeks or chin can also be affected (Adee AC
1993). The characteristic skin changes can occur in as little as 3 minutes. An episode can last from a few
minutes to several hours (NIAMS 2001), although episodes may last longer in people who have connective
tissue disorders such as scleroderma (Dziankowska-Bartkowiak B et al 2004).
- No matter what the underlying cause is, it is known that episodes of RS trigger significant free-radical nerve
damage in affected tissues. During RS, the blood flow is restricted, then restored. This causes ischemic
reperfusion injury, the same type of injury that can occur after a stroke, when the returning blood flow to the
brain causes additional damage. In RS, the ischemic reperfusion injury (which generates high levels of free
radicals that attack the endothelium in arteries and surrounding tissue) causes scar tissue to form in the
connective tissue (Simonini G et al 2000). This may help explain why RS is frequently associated with
autoimmune connective tissue disorders such as scleroderma, lupus, and arthritis (Ziegler S et al 2003). In about
20 percent of cases, RS is the first indication of a more serious connective tissue disorder such as scleroderma,
lupus, or arthritis, which means that the conditions of patients who have RS should be closely monitored for
these conditions (Grassi W et al 1998; Ho M et al 1998; Ziegler S et al 2003).
- Episodes of RS are unpredictable and difficult to reproduce accurately in a clinical setting (Bornmyr S et al
2001). RS can remain dormant for years, only to resurface suddenly in response to infection, fatigue, or stress. If
RS progresses, permanently decreased blood flow to the affected area can cause fingers to become thin and
tapered, with smooth shiny skin and slow-growing nails. Often the most serious consequence is loss of
sensitivity in the affected extremity. However, more severe cases of secondary RS can result in tissue death,
finger deformity, skin ulceration, or gangrene (Lavery JP et al 1992). RS can also affect the lungs. When the
lungs are affected, breathing cold air triggers a coughing attack (ISN 2005). Vasospasm may also affect the
heart, lungs, and kidneys (Ho M et al 1998).
- Diagnosing RS
Diagnosing RS is complicated because it can be mistaken for other conditions such as carpal tunnel syndrome,
vascular disease, or thoracic outlet syndrome (Lavery JP et al 1992). Therefore, physicians diagnose RS based
on the presence of some of the following factors (NIAMS 2001):
Periodic attacks of cyanosis
A negative antinuclear antibody test result, which demonstrates the absence of lupus
A normal erythrocyte sedimentation rate, which demonstrates the absence of major systemic inflammation
Although it is difficult to cause an attack of RS in a doctor’s office (Bornmyr S et al 2001), submerging the patient’
s hands in ice, recording the time it takes for normal color to return to the hands, and performing a vascular
assessment may determine the severity of RS.
- Because RS may be an important marker of more serious disease conditions, a full blood laboratory panel
should be performed to rule out underlying autoimmune disorders, malignancies, kidney or liver dysfunction,
and syndromes that affect the blood or circulation (Lavery JP et al 1992). In particular, an antinuclear antibody
test and erythrocyte sedimentation rate should be performed to assess potential autoimmune conditions.
Diagnosis of secondary RS includes periodic episodes of cyanosis, a positive antinuclear antibody test result,
and an abnormal erythrocyte sedimentation rate (NIAMS 2001).
- Conventional Treatment of RS
Treatment of RS is determined by type. In primary RS, conventional treatment is often conservative, using self-
help strategies such as preventing attacks and reducing symptoms. Pharmacological treatment is rarely
required and, unfortunately, antioxidant therapy is rarely recommended. When necessary, calcium channel
blockers are considered the safest and most effective drugs. They relax smooth muscle and dilate small blood
vessels, reducing the frequency and severity of attacks in primary and secondary RS (NIAMS 2001).
- We have shown only a couple of kinds of arthritis and their connection to Glutathione.
- At any event Arthritis is an Autoimmune Disease,
- Glutathione the molecule in the body is the most efficient at Balancing the Immune System and
thus making the system strong to fight disease.
- In any event anyone who is suffering from any kind of Arthritis would benefit hugely from the
consumption of GSH Immunity, an efficient Glutathione precursor.
Please contact by phone or email
if you are interested in purchasing GSH IMMUNITY or needing more information,
I do hope that we have satisfied your need for answers in this problem of the Immune System.
Thank you for reading this and hope to hear from you.
250 - 422 - 3163 ( Mountain time )
least.
Arthritis ('arth' meaning joint, 'itis' meaning inflammation) isn't a one-note story or even a few variations on a
single theme; it actually consists of more than 100 different conditions. These can be anything from relatively
mild forms of tendinitis (as in 'tennis elbow') and bursitis to crippling systemic forms, such as rheumatoid
arthritis. There are pain syndromes like fibromyalgia and arthritis-related disorders, such as systemic lupus
erythematosus, that involve every part of the body. There are forms of the disease, such as gout, that almost
nobody connects with arthritis, and there are other conditions - like osteoarthritis, the misnamed 'wear and tear'
arthritis - that a good many people think is the only form of the disease.
True, many older people do have arthritis, but it's not just a disease of the old. Some forms of arthritis affect
children still in diapers, while thousands of people are stricken in the prime of their lives. The common
denominator for all these conditions is joint and musculoskeletal pain, which is why they are grouped together
as 'arthritis.' Often that pain is a result of inflammation of the joint lining.
Inflammation is involved in many forms of arthritis. It is the body's natural response to injury. The warning
signs that inflammation presents are redness, swelling, heat and pain. These are the same kinds of reaction the
body has to a sliver in the hand, for example. When a joint becomes inflamed, it may get any or all of these
symptoms. This can prevent the normal use of the joint and therefore it can cause the loss of function of that
joint.
Anatomy of a Joint
There are more than 100 joints connecting the body's
206 bones. Most of the major bone connections in the
body are joints designed to allow a broad range of motion.
There are different kinds for different functions:
ball-and-socket (hips and shoulders), saddle joints (which
connect thumb to hand), hinge joints (fingers and knees)
or pivot joints (wrists).
Tied together by ligaments, the bones of joints are capped
with a smooth substance called cartilage. This tough elastic
material acts as a shock absorber and allows the bone ends
to glide smoothly across each other. If the cartilage is
destroyed (as in osteoarthritis), the bones of a joint can
grind against each other causing pain, loss of mobility, deformity and dysfunction.
Between the bones is a joint cavity, which gives the bones room to move. The joint space between two bones
is enclosed by a capsule that's flexible, yet strong enough to protect the joint against dislocation. The inner
lining of this capsule, the synovium, produces a thick fluid that lubricates and nourishes the joint. In many forms
of arthritis, the synovium becomes inflamed and thickened, producing extra fluid which contains inflammatory
cells. The inflamed synovium and fluid can damage the cartilage and underlying bone.
Some people think that there are only a couple of kinds of Arthritis, However make no mistake.... there are 100
FOLD and probably more to be added to this list.......
Achilles tendinitis Achondroplasia Acromegalic arthropathy
Adhesive capsulitis
Adult onset Still's disease Ankylosing spondylitis Anserine bursitis
Avascular necrosis
Behcet's syndrome Bicipital tendinitis Blount's disease
Brucellar spondylitis
Bursitis Calcaneal bursitis Calcium pyrophosphate dihydrate (CPPD)
Crystal deposition disease Caplan's syndrome Carpal tunnel syndrome
Chondrocalcinosis
Chondromalacia patellae Chronic synovitis Chronic recurrent multifocal osteomyelitis
Churg-Strauss syndrome Cogan's syndrome Corticosteroid-induced osteoporosis
Costosternal syndrome CREST syndrome Cryoglobulinemia
Degenerative joint disease
Dermatomyositis Diabetic finger sclerosis Diffuse idiopathic skeletal hyperostosis
(DISH)
Discitis Discoid lupus erythematosus Drug-induced lupus
Duchenne's muscular dystrophy
Dupuytren's contracture Ehlers-Danlos syndrome Enteropathic arthritis
Epicondylitis
Erosive inflammatory osteoarthritis Exercise-induced compartment syndrome
Fabry's disease Familial Mediterranean fever Farber's lipogranulomatosis
Felty's syndrome
Fibromyalgia Fifth's disease Flat feet
Foreign body synovitis
Freiberg's disease Fungal arthritis Gaucher's disease Giant
cell arteritis
Gonococcal arthritis Goodpasture's syndrome Gout Granulomatous arteritis
Hemarthrosis
Hemochromatosis Henoch-Schonlein purpura Hepatitis B surface antigen disease Hip
dysplasia
Hurler syndrome Hypermobility syndrome Hypersensitivity vasculitis
Hypertrophic osteoarthropathy
Immune complex disease Impingement syndrome Jaccoud's arthropathy Juvenile
ankylosing spondylitis
Juvenile dermatomyositis Juvenile rheumatoid arthritis Kawasaki disease
Kienbock's disease
Legg-Calve-Perthes disease Lesch-Nyhan syndrome Linear scleroderma
Lipoid dermatoarthritis
Lofgren's syndrome Lyme disease Malignant synovioma
Marfan's syndrome
Medial plica syndrome Metastatic carcinomatous arthritis Mixed connective tissue disease
(MCTD)
Mixed cryoglobulinemia Mucopolysaccharidosis Multicentric
reticulohistiocytosis
Multiple epiphyseal dysplasia Mycoplasmal arthritis Myofascial pain syndrome
Neonatal lupus
Neuropathic arthropathy Nodular panniculitis Ochronosis
Olecranon bursitis
Osgood-Schlatter's disease Osteoarthritis Osteochondromatosis
Osteogenesis imperfecta
Osteomalacia Osteomyelitis Osteonecrosis
Osteoporosis
Overlap syndrome Pachydermoperiostosis Paget's disease of bone
Palindromic rheumatism
Patellofemoral pain syndrome Pellegrini-Stieda syndrome Pigmented villonodular synovitis
Piriformis syndrome
Plantar fasciitis Polyarteritis nodos Polymyalgia rheumatica
Polymyositis
Popliteal cysts Posterior tibial tendinitis Pott's disease
Prepatellar bursitis
Prosthetic joint infectio Pseudoxanthoma elasticum Psoriatic arthritis
Raynaud's phenomenon
Reactive arthritis/Reiter's syndrome Reflex sympathetic dystrophy syndrome
Relapsing polychondritis Retrocalcaneal bursitis Rheumatic fever
Rheumatoid arthritis
Rheumatoid vasculitis Rotator cuff tendinitis Sacroiliitis
Salmonella osteomyelitis
Sarcoidosis Saturnine gout Scheuermann's osteochondritis
Scleroderma
Septic arthritis Seronegative arthritis Shigella arthritis
Shoulder-hand syndrome
Sickle cell arthropathy Sjogren's syndrome Slipped capital femoral epiphysis
Spinal stenosis
Spondylolysis Staphylococcus arthritis Stickler syndrome
Subacute cutaneous lupus
Sweet's syndrome Sydenham's chorea Syphilitic arthritis Systemic
lupus erythematosus (SLE)
Takayasu's arteritis Tarsal tunnel syndrome Tennis elbow
Tietse's syndrome
Transient osteoporosis Traumatic arthritis Trochanteric bursitis
Tuberculosis arthritis
Arthritis of Ulcerative colitis Undifferentiated connective tissue syndrome (UCTS)
Urticarial vasculitis
Viral arthritis Wegener's granulomatosis Whipple's disease
Wilson's disease
Yersinial arthritis
ARTICLE ON RHEUMATOID ARTHRITIS
- Rheumatoid Arthritis: New Discoveries Against Joint Pain and RA Symptoms
Individuals struggling with the pain and symptoms of Rheumatoid Arthritis, RA, will want to know about NEW
medical discoveries that are helping many people to significantly reduce and even clear their SYMPTOMS,
especially JOINT PAIN!
- One of these discoveries is about BALANCING instead of SUPPRESSING the immune system with immune
suppressant drugs -- and instead, how to CALM the immune and "bring it back into line" when it is "out of
whack."
- RA is considered to be an autoimmune disease, where the immune system is "over the top," and attacks the
joints, which causes pain and dysfunction -- but there is more to it!
Why Balance, Not Suppress Your Immune System?
- If you have Rheumatoid Arthritis, it is important that you know about the discovery that your immune can be
both "UNDER-active" and "OVER-active" at the same time!
- In fact, scientists have reported that with RA there are both "OVER-active" B cells and "under-active" T cells.
- This means that ... the "OVER-activity" is "PICKING ON" the joints, causing inflammation and pain.
- On the other hand, the "UNDER-activity" represents a weakened ability to deal with "ANTIGENS," i.e. to "MOP
UP" excess free radicals and "OXIDATIVE STRESS."
- This UNDER ACTIVITY also eventually results in tissue damage and increased inflammation and pain!
Best "Food for Your Immune?"
- For healing your RA, you need to both STRENGTHEN the UNDERactive parts of your immune, as well as CALM
the OVERactive immune responses.
- Just using IMMUNE SUPPRESSANT DRUGS does not really solve the problem, because this only addresses
one part of the equation.
- How to RE-BALANCE the immune to restore its natural SELF-REGULATING capacity? There is a NATURAL
DISCOVERY, a protein that improves the body's glutathione levels.
GLUTATHIONE : Why is it the key?
- Scientific data is pointing to a molecule called Glutathione as being key to the regulation of the immune
system -- both its ups AND its downs!
- In fact...there are scientists who have demonstrated a clear IMPROVEMENT OF INFLAMMATION after raising
Glutathione in affected tissues.
- Furthermore, this new discovery is noteworthy to people with Rheumatoid Arthritis now, because it has
recently become known that glutathione levels are best raised with precursors such as GSH-IMMUNITY.
Nutrition -- Not Just a Pill
- Glutathione is a fragile protein which is destroyed in stomach juices, there for pills cannot improve your
body's glutathione levels.
Dr. Bounous' "Back To Nature" Discovery:
- It was Dr. Bounous at McGill University in Montreal, who, after two decades of research, "Ended up identifying
the remarkable properties of some proteins that turned out to be the same as the three proteins in mothers’
breast milk.”
“It was a back-to-nature call,” according to Dr. Bounous.
- His discovery was -- the secret of nature to provide a cysteine-rich protein as the natural building block, or
NUTRITIONAL precursor, to making Glutathione.
- Anyone with Rheumatoid Arthritis OR ANY ARTHRITIS can benefit from this discovery by increasing their
Glutathione levels safely and naturally, with CYSTEINE-RICH protein to reduce inflammation and pain.
No Pain Killers Are Safe, Say Scientists
- Why use supplements to heal the body rather than rely on pain killers? A recent study shows that most
prescription and over-the-counter painkillers increase the risk of heart attacks. In the wake of the largest study
to date showing most nonsteroidal anti-inflammatory drugs (NSAIDs) -- including ibuprofen, naproxen, and
Celebrex -- increase the risk of heart attacks in people with arthritis, experts are once again urging all involved
to weigh their individual risks when choosing a painkiller.
- "This is a class effect of all the drugs," says researcher Gurkirpal Singh, MD, professor of medicine,
immunology, and rheumatology at Stanford University Medical School about his study presented at the Annual
European Congress of Rheumatology in Vienna, Austria.
Acetaminophen has been shown to deplete Glutathione from lung tissue.
Raynaud's Syndrome
- Raynaud’s syndrome (RS) can be a debilitating condition that causes periods of severely restricted blood flow
to the fingers and toes (and sometimes to other parts of the body such as the nose or ears). In the worst case
scenario, this can result in amputation of the damaged digits. The causes of RS remain a mystery in many cases.
-The disease causes significant free-radical nerve damage in the affected tissues. This damage leads to local
endothelial dysfunction, thickening of the arterial walls, and the formation of scar tissue, or fibrosis (Simonini G
et al 2000). RS is closely associated with more serious diseases (especially scleroderma, a connective tissue
disorder). Many scientists believe that RS may be the initial diagnosis, before the actual diagnosis of
scleroderma is recognized. Other diseases associated with RS include systemic lupus erythematosus and
arthritis.
- In each case, RS may contribute to the more serious disease by encouraging the formation of scar tissue in
the connective tissue and through damage to arteries. Therefore, it is crucial that patients who have RS pursue
aggressive ANTIOXIDANT THEARPY to lower their risk of developing a more serious condition.
- RS typically affects the small blood vessels in the fingers and toes but can affect those in the ears, nose, and
tip of the tongue as well (Adee AC 1993; Awami M et al 2004a,b; NIAMS 2001). During episodes of RS, the
affected area may become painful and turn blue (NIAMS 2001). RS that occurs in the absence of another disease
is referred to as primary RS (also sometimes called Raynaud’s disease or Raynaud’s syndrome). It is thought to
involve a localized defect in the arteries and arterioles that deliver blood to the extremities. Because RS is
associated with conditions, such as migraine headaches and angina, caused by spasms of blood vessels
(vasospasm), it may have a similar vasospastic mechanism.
- RS that occurs in the presence of other diseases is called secondary RS. Occupational RS is a common form of
secondary RS that results from using vibrating tools such as jackhammers (NIAMS 2001). Drugs or treatments
used to treat high blood pressure (beta blockers), migraine headaches (ergotamine-containing drugs), and
cancer (chemotherapy) have been known to cause RS (Merck 2005; NIAMS 2001). Oxidative Damage: RS’s
Lasting Effect
- In normal healthy tissue, blood flow to the skin is regulated by a complex system that includes neural signals,
hormones, and mediators released from circulating cells and blood vessels. Under normal circumstances, when
a person is exposed to cold or is under emotional stress, arterioles constrict to return blood flow to the core of
the body, for warmth and protection (NIAMS 2001). This reaction is regulated by vasoconstrictive agents such as
endothelin 1 (Nakamura H et al 2003; Rajagopalan S et al 2003a) and factors that impair production of nitric
oxide, a potent vasodilator (Generini S et al 2005).
-In individuals with RS, the normal reaction is exaggerated—blood circulation in the arterioles is greatly
restricted, resulting in a visible progression of symptoms as blood flow to the affected areas drops. Skin first
turns white as it is deprived of blood, then turns blue (cyanosis) because of the lack of blood and oxygen, and
then has localized red flushing as the blood returns to the affected area (Browne BJ et al 1995). This progression
may be accompanied at first by a loss of sensation in the affected extremities, followed by a prickling,
throbbing, or tingling sensation as circulation returns (NIAMS 2001).
Skin changes may migrate, moving from one finger to the next, sometimes even involving the thumb (Pistorius
MA et al 1995). The tip of the nose, the earlobes, and (rarely) the cheeks or chin can also be affected (Adee AC
1993). The characteristic skin changes can occur in as little as 3 minutes. An episode can last from a few
minutes to several hours (NIAMS 2001), although episodes may last longer in people who have connective
tissue disorders such as scleroderma (Dziankowska-Bartkowiak B et al 2004).
- No matter what the underlying cause is, it is known that episodes of RS trigger significant free-radical nerve
damage in affected tissues. During RS, the blood flow is restricted, then restored. This causes ischemic
reperfusion injury, the same type of injury that can occur after a stroke, when the returning blood flow to the
brain causes additional damage. In RS, the ischemic reperfusion injury (which generates high levels of free
radicals that attack the endothelium in arteries and surrounding tissue) causes scar tissue to form in the
connective tissue (Simonini G et al 2000). This may help explain why RS is frequently associated with
autoimmune connective tissue disorders such as scleroderma, lupus, and arthritis (Ziegler S et al 2003). In about
20 percent of cases, RS is the first indication of a more serious connective tissue disorder such as scleroderma,
lupus, or arthritis, which means that the conditions of patients who have RS should be closely monitored for
these conditions (Grassi W et al 1998; Ho M et al 1998; Ziegler S et al 2003).
- Episodes of RS are unpredictable and difficult to reproduce accurately in a clinical setting (Bornmyr S et al
2001). RS can remain dormant for years, only to resurface suddenly in response to infection, fatigue, or stress. If
RS progresses, permanently decreased blood flow to the affected area can cause fingers to become thin and
tapered, with smooth shiny skin and slow-growing nails. Often the most serious consequence is loss of
sensitivity in the affected extremity. However, more severe cases of secondary RS can result in tissue death,
finger deformity, skin ulceration, or gangrene (Lavery JP et al 1992). RS can also affect the lungs. When the
lungs are affected, breathing cold air triggers a coughing attack (ISN 2005). Vasospasm may also affect the
heart, lungs, and kidneys (Ho M et al 1998).
- Diagnosing RS
Diagnosing RS is complicated because it can be mistaken for other conditions such as carpal tunnel syndrome,
vascular disease, or thoracic outlet syndrome (Lavery JP et al 1992). Therefore, physicians diagnose RS based
on the presence of some of the following factors (NIAMS 2001):
Periodic attacks of cyanosis
A negative antinuclear antibody test result, which demonstrates the absence of lupus
A normal erythrocyte sedimentation rate, which demonstrates the absence of major systemic inflammation
Although it is difficult to cause an attack of RS in a doctor’s office (Bornmyr S et al 2001), submerging the patient’
s hands in ice, recording the time it takes for normal color to return to the hands, and performing a vascular
assessment may determine the severity of RS.
- Because RS may be an important marker of more serious disease conditions, a full blood laboratory panel
should be performed to rule out underlying autoimmune disorders, malignancies, kidney or liver dysfunction,
and syndromes that affect the blood or circulation (Lavery JP et al 1992). In particular, an antinuclear antibody
test and erythrocyte sedimentation rate should be performed to assess potential autoimmune conditions.
Diagnosis of secondary RS includes periodic episodes of cyanosis, a positive antinuclear antibody test result,
and an abnormal erythrocyte sedimentation rate (NIAMS 2001).
- Conventional Treatment of RS
Treatment of RS is determined by type. In primary RS, conventional treatment is often conservative, using self-
help strategies such as preventing attacks and reducing symptoms. Pharmacological treatment is rarely
required and, unfortunately, antioxidant therapy is rarely recommended. When necessary, calcium channel
blockers are considered the safest and most effective drugs. They relax smooth muscle and dilate small blood
vessels, reducing the frequency and severity of attacks in primary and secondary RS (NIAMS 2001).
- We have shown only a couple of kinds of arthritis and their connection to Glutathione.
- At any event Arthritis is an Autoimmune Disease,
- Glutathione the molecule in the body is the most efficient at Balancing the Immune System and
thus making the system strong to fight disease.
- In any event anyone who is suffering from any kind of Arthritis would benefit hugely from the
consumption of GSH Immunity, an efficient Glutathione precursor.
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I do hope that we have satisfied your need for answers in this problem of the Immune System.
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